Gesquière L, Loreau N, Blache D
INSERM CJF 93-10, Laboratoire de Biochimie des Lipoprotéines, Université de Bourgogne, Dijon, France.
Free Radic Biol Med. 1997;23(4):541-7. doi: 10.1016/s0891-5849(97)00114-7.
One of the proposed antiatherogenicity role of high-density lipoproteins (HDL) is believed to stimulate removal of cholesterol from the peripheral cells back to the liver for excretion. We have investigated the effects of oxidation-related modifications of HDL on their ability to stimulate cholesterol efflux from cultured cells. Human HDL (HDL3, 1.13 < d < 1.21 g/ml) have been modified either by malondialdehyde or by copper-mediated oxidation (Ox-HDL3). Compared with native HDL3, the modified HDL3 resulted in a significantly reduced efflux of labeled cholesterol from preloaded macrophages (P388D1 cell line). Analysis of lipid composition of Ox-HDL3 by gas chromatography revealed the presence of oxysterols (OS). Enrichment of native HDL3 with oxysterols resulted in a reduced capacity to stimulate cholesterol efflux. The reduced ability of OS-enriched HDL3 to elicit cholesterol efflux may contribute to cellular cholesterol accumulation and subsequently to atherosclerosis.
